?/ANTI-? COMPLEXES: STAPHYLOCOCCAL AUREUS PHAGE G1 ORF67

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• 批准号: 8169306
• 负责人: Seth A. Darst
• 金额: $ 0.2万
• 依托单位: CORNELL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8169306
• 关键词: Bacteria; Bacteriophages; Binding; Biology; C-terminal; Cell physiology; Complex; Computer Retrieval of Information on Scientific Projects Database; Cues; Environment; Funding; Genetic Transcription; Goals; Grant; Growth; Institution; Proteins; Regulation; Regulon; Research; Research Personnel; Resources; Response Elements; Role; Signal Transduction; Source; Staphylococcus aureus; Structure; United States National Institutes of Health; high throughput screening; inhibitor/antagonist; pathogen; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Bacterial transcription depends on a primary (group 1) ¿ that is essential for viability. In addition, most bacteria contain alternative ¿'s that control regulons in response to environmental cues. Regulation of ¿ activity is a major mechanism by which bacteria respond to their environment. Many alternative ¿'s are regulated by anti-¿ factors. Despite the structural conservation of ¿'s, anti-¿'s are structurally and functionally diverse, serving as the key response elements to sense and signal environmental cues to the core transcriptional apparatus via the alternative ¿'s. In addition to modulation of ¿ function by cellular anti-¿ factors, many bacteriophages have evolved ingenious mechanisms to inhibit and/or appropriate the host transcription apparatus. The primary ¿ (¿A) of the gram-positive pathogen Staphylococcus aureus (Sau) is targeted by phage proteins that inhibit bacterial growth. Phage G1 ORF67 was identified in a high-throughput screen as a transcriptional inhibitor that binds to the C-terminal domain (domain 4) of Sau ¿A (¿A4). Our goal is to determine the co-crystal structure of G1 ORF67 with Sau ¿A4, and to explore the functional mechanism through which ORF67 inhibits Sau transcription as well as it's role in phage G1 biology.

该副本是使用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这是调查员的机构。 细菌转录取决于对生存力至关重要的初级（第1组）。此外，大多数细菌都含有替代性，以响应环境线索来控制法规。活动的调节是细菌对其环境反应的主要机制。许多替代方案都受到抗因子的调节。尽管``''的结构保守性在结构和功能上是多样的，它是通过替代方案对核心转录设备的感官和信号环境线索的关键响应要素。 除了通过细胞抗因子对功能的调节外，许多细菌噬菌体还发展了巧妙的机制以抑制和/或适当的宿主转录设备。革兰氏阳性病原体金黄色葡萄球菌（SAU）的一级（a）的靶向噬菌体蛋白抑制细菌生长。噬菌体G1 ORF67在高通量屏幕上被鉴定为与Sau»a（«a4）的C末端结构域（域4）结合的转录抑制剂。我们的目标是确定G1 ORF67与A4的共结晶结构，并探索ORF67抑制SAU转录以及在噬菌体G1生物学中的作用的功能机制。